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Infection and Immunity, September 2005, p. 5420-5425, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5420-5425.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Involvement of Toll-Like Receptor 2 in Experimental Invasive Pulmonary Aspergillosis

Viviane Balloy,1 Mustapha Si-Tahar,1 Osamu Takeuchi,2 Bruno Philippe,3 Marie-Anne Nahori,4 Myriam Tanguy,5 Michel Huerre,5 Shizuo Akira,2 Jean-Paul Latgé,3 and Michel Chignard1*

Unité de Défense Innée et Inflammation, Inserm E336, Institut Pasteur, 25, rue du Dr Roux, 75015 Paris, France,1 Department of Host Defense, Research Institute For Microbial Diseases, Osaka University, Osaka, Japan,2 Unité des Aspergillus, Institut Pasteur, 25, rue du Dr Roux, 75015 Paris, Franc,3 Unité de Bactériologie Moléculaire et Médicale, Institut Pasteur, 28, rue du Dr Roux, 75015, Paris, France,4 Unité de Recherche et d'Expertise Histotechnologie et Pathologie, Institut Pasteur, 25, rue du Dr Roux, 75015 Paris, France5

Received 23 December 2004/ Returned for modification 6 January 2005/ Accepted 15 March 2005

Aspergillus fumigatus, an opportunistic fungal pathogen, causes severe and usually fatal invasive pulmonary aspergillosis in immunocompromised hosts. Interestingly, Drosophila cells lacking the Toll protein are prone to A. fumigatus infection. In the current study, we looked for the involvement of Toll-like receptor 2 (TLR2) in the recognition of A. fumigatus by analyzing the in vivo and ex vivo responses of immunocompromised TLR2–/– and TLR2+/+ mice to this fungus. Upon intratracheal administration of conidia, survival and tumor necrosis factor alpha (TNF-{alpha}), interleukin-12, and macrophage inhibitory protein-2 alpha concentrations in the airspaces of TLR2–/– mice were significantly lower than those of TLR2+/+ animals. In vitro analysis of TNF-{alpha} production by conidia-challenged alveolar macrophages from TLR2–/– revealed a significant deficiency in comparison with macrophages from TLR2+/+ mice. Infected TLR2–/– mice also have a higher respiratory distress and a higher pathogen burden than TLR2+/+ mice. These data demonstrate that TLR2 plays a significant role in the defense of the host against A. fumigatus infection.

* Corresponding author. Mailing address: Unité de Défense Innée et Inflammation, Inserm E336, Institut Pasteur, 25, rue du Dr Roux, 75015 Paris, France. Phone: (33 1) 45 68 86 88. Fax: (33 1) 45 68 87 03. E-mail: chignard{at}pasteur.fr.

Editor: T. R. Kozel

Infection and Immunity, September 2005, p. 5420-5425, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5420-5425.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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